Zdenek Vrozina Profile picture
Mar 31 13 tweets 2 min read Read on X
Hidden driver of mortality. A new study makes an uncomfortable point very clear. Respiratory viruses are probably involved in far more deaths than we usually recognize in day-to-day clinical practice or in official cause-of-death statistics🧵
Across 4 influenza seasons, a respiratory virus was found post mortem in 36.4% of deceased people. Influenza alone was present in 11.0%. It was not just flu either - rhinoviruses, common human coronaviruses, and RSV were also frequent.
The most striking part is how much was missed before death. Among people with influenza detected post mortem, only 17% had been diagnosed with influenza while alive.
That matters because what gets recorded as cardiac death, respiratory failure, or general decline may, in many cases, have had a hidden viral trigger helping push a frail patient over the edge.
The study does not claim every virus detected was the direct cause of death - but it strongly suggests we are overlooking a major part of the story.
These viruses are not harmless background noise. They can worsen an already fragile situation, destabilize chronic illness, and become part of fatal outcomes even when they never make it into the headline diagnosis.
The signal was especially strong in long-term care facilities, where any respiratory virus was found in 52.3% of deceased residents!
That is exactly where transmission is easier, patients are more vulnerable, and missed infections can carry the heaviest consequences.
So ignoring such a high prevalence would be a mistake. These infections are being underdiagnosed in life and undercounted in death.
The practical takeaway is simple.
Test more, think of viral etiologies more often, and stop assuming that if a patient looks cardiac, pulmonary, or just frail, infection is no longer central to what is happening.
And this study comes from the pre-COVID era. Since then, SARS-CoV-2 arrived. More severe, poorly tested, devastating in care homes, and far too often met with delayed, limited, or badly implemented antiviral access.
If we were already underestimating how flu and other respiratory viruses contribute to fatal decline, COVID only made that blind spot bigger. We need better testing, earlier recognition, and much better treatment access for the people at highest risk.
Trobajo-Sanmartín at al., Prevalence of influenza and other respiratory viral infections in deceased persons: a population-based observational study over four influenza seasons. clinicalmicrobiologyandinfection.org/article/S1198-…

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More from @ZdenekVrozina

Mar 30
A bystander apoptosis. The study in Nature argues that Omicron can drive the death of nearby, uninfected T cells. This paper shows an HIV-like pattern of immunopathology.🧵
A new paper suggests something important about severe Omicron cases.
The damage may not come only from the cells the virus infects directly.
It may also come from the immune cells caught in the crossfire.
The study argues that Omicron can drive the death of nearby, uninfected T cells.
That matters, because T cells are central to immune defense.
So the story is bigger than how much virus is inside a given cell.
Read 17 tweets
Mar 28
Why might insulin resistance go up after COVID? Probably not because of one single cause, but because of a whole network of inflammatory and metabolic changes. A new narrative review.🧵
Some people seem to have worse blood sugar control and higher insulin resistance after COVID. What this paper argues is interesting - it’s probably not one clean, simple mechanism. It’s more like a web of biological processes that can keep reinforcing each other.
The authors first separate acute COVID from the longer post-COVID phase. In the acute stage, part of the problem may be in the pancreas itself. SARS-CoV-2 may affect the cells that make insulin. But when symptoms linger, they argue insulin resistance becomes the bigger story.
Read 21 tweets
Mar 25
Patient-derived IgG in Long COVID appears functionally pathogenic - and in some cases, this autoreactivity persists for years🧵
At the heart of the paper is a pretty important question. We already know that Long COVID has often been linked to autoimmunity, but that alone does not tell us whether these antibodies are actually doing harm or whether they are simply a byproduct of the illness.
What the authors tried to test here was the functional side of that question - can these antibodies themselves trigger measurable effects? They purified IgG from the plasma of Long COVID patients and transferred those into mice. They then looked for changes in sensory and behavioral testing.
Read 12 tweets
Mar 24
One of the most interesting theories in ME/CFS - and in Long Covid too - is the IDO metabolic trap idea from Robert Phair and Ron Davis. Not because it’s proven, but because it’s one of the few theories that tries to explain why people get stuck.
It doesn’t treat post viral illness as vague bad luck, or as a list of symptoms floating around. It asks a harder question - what if the body isn’t failing to recover - what if it’s been pushed into the wrong stable state?
The theory centers on tryptophan metabolism. Normally tryptophan is processed down the kynurenine pathway, and the enzymes IDO1 and IDO2 help regulate that flow. Phair and Davis asked whether, under the wrong conditions, that system could basically jam.
Read 24 tweets
Mar 23
The real headline here is simple - this preprint study set immunity debt against SARS-CoV-2 as rival explanations for rising invasive strep - and only one of them held up in the data🧵
This study asks a very specific question. What best explains the post-pandemic rise in invasive group A streptococcal infections (iGAS)?
Is it mainly immunity debt - the idea that reduced exposure during pandemic restrictions left people more vulnerable - or is it more consistent with the effects of prior SARS2 infection? The authors set those two explanations directly against each other and try to see which one the data actually support.
Read 17 tweets
Mar 23
An interesting new review proposes that Long COVID is not just about what keeps the immune system on, but also about what fails to turn it off🧵
This review proposes a striking model for Long COVID. A self sustaining loop in which lingering danger signals keep innate immunity activated, tissue injury generates new inflammatory cues, and the normal transition from inflammation to repair never fully happens.
1. After the acute infection is over, the body may still be exposed to signals that look dangerous to the innate immune system. These could include leftover SARS2 material, reactivated latent viruses, microbial products leaking across damaged mucosal barriers like the gut or nasopharynx, distress signals released by injured tissues themselves.
Read 22 tweets

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